Substituting whole grains for refined grains in a 6-wk randomized trial has a modest effect on gut microbiota and immune and inflammatory markers of healthy adults

Observational studies suggest an inverse association between whole-grain (WG) consumption and inflammation. However, evidence from interventional studies is limited, and few studies have included measurements of cell-mediated immunity. We assessed the effects of diets rich in WGs compared with refin...

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Published inThe American journal of clinical nutrition Vol. 105; no. 3; pp. 635 - 650
Main Authors Vanegas, Sally M, Meydani, Mohsen, Barnett, Junaidah B, Goldin, Barry, Kane, Anne, Rasmussen, Helen, Brown, Carrie, Vangay, Pajau, Knights, Dan, Jonnalagadda, Satya, Koecher, Katie, Karl, J Philip, Thomas, Michael, Dolnikowski, Gregory, Li, Lijun, Saltzman, Edward, Wu, Dayong, Meydani, Simin Nikbin
Format Journal Article
LanguageEnglish
Published United States American Society for Clinical Nutrition, Inc 01.03.2017
American Society for Nutrition
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Summary:Observational studies suggest an inverse association between whole-grain (WG) consumption and inflammation. However, evidence from interventional studies is limited, and few studies have included measurements of cell-mediated immunity. We assessed the effects of diets rich in WGs compared with refined grains (RGs) on immune and inflammatory responses, gut microbiota, and microbial products in healthy adults while maintaining subject body weights. After a 2-wk provided-food run-in period of consuming a Western-style diet, 49 men and 32 postmenopausal women [age range: 40-65 y, body mass index (in kg/m ) <35] were assigned to consume 1 of 2 provided-food weight-maintenance diets for 6 wk. Compared with the RG group, the WG group had increased plasma total alkyresorcinols (a measure of WG intake) ( < 0.0001), stool weight ( < 0.0001), stool frequency ( = 0.02), and short-chain fatty acid (SCFA) producer [false-discovery rate (FDR)-corrected = 0.25] but decreased pro-inflammatory (FDR-corrected = 0.25). Changes in stool acetate ( = 0.02) and total SCFAs ( = 0.05) were higher in the WG group than in the RG group. A positive association was shown between and acetate (FDR-corrected = 0.002) or butyrate (FDR-corrected = 0.005). We also showed that there was a higher percentage of terminal effector memory T cells ( = 0.03) and LPS-stimulated ex vivo production of tumor necrosis factor-α ( = 0.04) in the WG group than in the RG group, which were positively associated with plasma alkylresorcinol concentrations. The short-term consumption of WGs in a weight-maintenance diet increases stool weight and frequency and has modest positive effects on gut microbiota, SCFAs, effector memory T cells, and the acute innate immune response and no effect on other markers of cell-mediated immunity or systemic and gut inflammation. This trial was registered at clinicaltrials.gov as NCT01902394.
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Present address: Kerry Inc., 3400 Millington Road, Beloit, WI 53511.
Supplemental Tables 1–8 are available from the “Online Supporting Material” link in the online posting of the article and from the same link in the online table of contents at http://ajcn.nutrition.org.
Present address: Boston University School of Public Health, 801 Massachusetts Avenue, Boston, MA 02118.
Any opinions, findings, conclusions, or recommendations expressed in this article are those of the authors and do not necessarily reflect the views of the USDA.
Supported by the Bell Institute of Health and Nutrition, General Mills Inc., and by the USDA/Agricultural Research Service (ARS) (agreement 58-1950-0-014). SMV was supported by a Stanley N Gershoff Scholarship from the Friedman School of Science and Policy, by a National Research Service Award from the National Institute of Diabetes and Digestive and Kidney Diseases T32 Research Training Program in Nutrition and Chronic Disease (grant 2T32DK062032-21), by an American Society for Nutrition 2012 Kraft Foods Inc. predoctoral fellowship, and by the USDA/ARS (agreement 58-1950-0-014). JPK was supported by the Science, Mathematics, and Research Transformation Defense Education Program.
Present address: US Army Research Institute of Environmental Medicine, 10 General Greene Avenue, Natick, MA 01760.
ISSN:0002-9165
1938-3207
1938-3207
DOI:10.3945/ajcn.116.146928